| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Outline of Final Research Achievements |
In this study, we evaluated the roles of inflammatory processes in cardiovascular remodeling. Using murine model of pressure-overload induced cardiac hypertrophy and fibrosis, we examined the roles of inflammatory macrophages during cardiac remodeling. We also established a murine model of pulmonary artery overflow vasculopathy, where we induced a volume shift of the pulmonary artery leading to the vascular remodeling. Based on the current model, we found that monocyte/ macrophages accumulate to the lung of overflow vasculopathy. We further examined the ischemic environment in fibroblasts activation. Through the genetic or pharmacological approaches, we found that hypoxia inducible factor mediated glycolytic reprograming elicits fibroblast activation. We also identified that serum starved environment accelerate collagen production in in vitro cultured fibroblasts. These results illuminate previously unidentified pathological processes which underlie cardiovascular remodeling.
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